1. Field of the Invention
This invention relates to a measuring and analyzing system, more particularly to a non-invasive system for measuring and analyzing the vasodilatation index to determine the endothelial function of blood vessels so as to serve as a reference index for coronary atherosclerosis.
2. Description of the Related Art
Cardiovascular diseases are still ranked among the top ten killers in Taiwan. Atherosclerosis and coronary arterial diseases often lead to myocardiac infarcts and heart failure, which are the major causes of death. Atherosclerosis is chiefly characterized by fat accumulation in parts of the vascular walls, and the fats are built up in the cells or in interstitial cells in the form of cholesterol or labile cholesterol. It is known that recurring impairment of endothelial cells and increased adipose infiltration are critical processes in the formation of atherosclerosis.
Endothelial cells are a layer of cells that adhere to the inside walls of arteries. These cells regulate their functions through nitric oxide (NO), a gaseous neurotransmitter responsible for signal transmission in living organisms. Nitric oxide not only is the most critical and essential signal transmitting gaseous substance in the cardiovascular system, it also has other functions. After generation by the innermost cells (endothelial cells) of the arteries, nitric oxide is quickly diffused to the smooth muscle cells under the blood vessels to inhibit contraction of vascular muscle cells to thereby result in arterial dilation. Thus, nitric oxide can be said to be a blood flow-mediated vasodilating substance capable of controlling distribution of blood and blood pressure in the blood vessels.
Endothelial cell dysfunction is the major initial step of atherosclerosis. Atherosclerosis risk factors, which include diabetes, hypertension, smoking, etc., can cause dysfunction of endothelial cells. When the endothelial cells are impaired, atherosclerosis is likely to result due to cholesterol buildup. As such, determination of the extent of endothelial cell dilation is the initial condition in the screening of atherosclerosis. Therefore, how to measure endothelial dysfunction in human beings, particularly with a non-invasive method, is a goal scientists are striving to achieve. At present, the most commonly used non-invasive method is measuring the vasodilatation of the posterior brachial artery after ischemia by ultrasonography. However, this method has limitations in that it is highly technique-dependent and highly variable. In addition, there has been developed a method of employing digital pulse to detect vasodilatation after inhalation of a beta-adrenergic agonist so as to measure the endothelial function. Although the latter method is quite simple and convenient, it has the limitation that the subject needs to inhale a bronchial dilator prior to measurement. Thus, this invention proposes a system for analyzing the endothelial function based on a measurement of the digital pulse to serve as a reference in the determination of atherosclerosis. To this end, the definition and significance of pulses as referred to herein will be described in the succeeding paragraphs.
A cardiac cycle is divided into systolic (contraction) and diastolic (relaxation) periods, and the heart beats rhythmically and cyclically. When the heart contracts, the relatively large pressure (systolic pressure) created by the ventricles forces a large amount of blood to flow into the aorta and, at the same time, drives the blood to flow along the arteries and arterioles into the peripheral vessels. This is the rapid ejection phase. During this phase, the input of blood into the proximal aorta (proximal to the heart) exceeds the blood output so that the volume of blood in the vessels increases, thereby resulting in drastic dilation of the vascular walls. This phase corresponds to the cycle from the pacemaker to the primary peak indicated in FIG. 1. Thereafter, the ventricles enter a slow ejection phase, during which the blood input into the proximal aorta is gradually lower than the blood output so that the volume of blood in the vessels decreases, thereby resulting in a pressure drop to cause contraction of the vascular walls. Since the arteries in the human body are closed loops, at the end of the ejection phase when the blood flows to the distal ends of the vessels, the blood rebounds so that some of the blood flows back into the aortic end, thereby causing a slight increase in the volume of blood in the proximal aorta, and a relative rise in the pressure. The vascular walls at this time will also experience a transient dilation. This corresponds to the position of the dicrotic peak shown in FIG. 1. Thereafter, the vascular walls will gradually return to their normal state before contraction. Accordingly, each contraction activity of the heart results in a rise in the pressure of the blood in the proximal aorta and dilation of the vascular walls. By using a suitable light-transmissible photo sensor element, a digital volume pulse (DVP) waveform as shown in FIG. 1 can be obtained. Shown at the upper left corner of FIG. 1 is a corresponding peripheral arterial pulse waveform obtained by electrocardiogram (ECG), which exhibited a time difference with the digital volume pulse.
During the systolic phase of the ventricles, the digital volume pulse is influenced by three factors: blood ejection velocity and volume of the ventricles, the elasticity (or compliance) of the vascular wall of the proximal aorta, and the peripheral resistance of blood vessels and blood to blood flow. If the blood volume at each pulsation increases, the vascular walls of the proximal aorta can sufficiently dilate, and the dilatory waves of the vascular walls during the systolic phase can be relatively large. When the elasticity of the vascular walls of the proximal aorta declines, the extent of dilation of the vascular walls during the systolic phase is limited by the declined elasticity and is therefore relatively low. As for an increase in the resistance of the peripheral vessels, it may result in reduced flow of blood from the aorta. Thus, during the systolic phase, the tendency of the blood volume in the proximal aorta to increase speeds up, the pressure rises, and the rate and extent of vascular dilation increase. On the other hand, with a decline in the resistance of the peripheral vessels, the tendency of the blood volume in the proximal aorta to increase slows down, and the rate and extent of pressure rise and vascular dilation decrease.
In addition, during transmission, the digital volume pulse is subjected to the influence of various factors that can cause changes in the waveform of the pulse. One is the fluctuation in the attenuation constants and the transmission rates of the harmonic wave components of the pulse itself which have different frequencies. Another important factor is wave reflection. The arterial system is a highly branched vascular system. The arteries decrease in cross-sectional area and the elasticity of the arterial walls become lower as well as they are farther away from the heart. When the volume pulse is being transmitted through the arteries, in case of variations in the cross-sectional area of the arteries (such as narrowing and branching of the arteries) or changes in the characteristic of the arterial walls, the pulse will be reflected in part, thereby resulting in variations in the pulse waveform.